Evidence map›Paper›PMID 40075503›Full record

ArticleRespiratory research2025

YAP/TAZ-mediated nuclear membrane rupture in promoting senescence of skeletal muscle associated with COPD.

Ge Gong, Shuping Shen, Shaoran Shen, Ran Wang, Tianping Zheng, Wei Xu, Jianqing Wu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Ge GongKey Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Shuping ShenKey Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Shaoran ShenKey Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Ran WangKey Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Tianping ZhengKey Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Wei XuKey Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China. ann_hsu@njmu.edu.cn.
Jianqing WuKey Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China. jwuny@njmu.edu.cn.

Funding

Applied research project unit of geriatric medicine clinical technology in Jiangsu Province LD2022001Jiangsu Province Capability Improvement Project through Science, Technology and Education No. CXZX202228Jiangsu Province Elderly Health Scientific Research Project LKM2024021The Major Natural Science Research Projects in Colleges and Universities of Jiangsu Province No. 22KJA320003the National Natural Science Foundation of China 82471605, 82171576
6 · The paper itself

Abstract

Patients with chronic obstructive pulmonary disease (COPD) often develop complications associated with sarcopenia; however, the underlying mechanisms remain unclear. Through a combination of in vitro and in vivo experiments, as well as bioinformatics analysis, our study identified YAP/TAZ as a key regulator of the aging phenotype in the skeletal muscle of COPD patients. In skeletal muscle affected by cigarette smoke-induced COPD, we observed significant reductions in YAP/TAZ levels, alongside markers indicative of skeletal muscle aging and dysfunction. Notably, overexpression of YAP/TAZ significantly improved these conditions. Our results suggest a novel mechanism whereby the maintenance of YAP/TAZ activity interacts with ACTR2 to preserve nuclear membrane integrity and reduce cytoplasmic dsDNA levels, thereby attenuating STING activation and cellular senescence. Additionally, we found that YAP is involved in the transcriptional regulation of the ACTR2 promoter region. Overall, preserving YAP/TAZ activity may help prevent skeletal muscle aging associated with COPD, representing a new strategy for intervening in COPD-related sarcopenia.

Indexed as

Adaptor Proteins, Signal TransducingCellular SenescenceMuscle, SkeletalNuclear EnvelopePulmonary Disease, Chronic ObstructiveTranscription FactorsAgedAnimalsCell Cycle ProteinsFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedSarcopeniaAdaptor Proteins, Signal TransducingCell Cycle ProteinsTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humanYAP1 protein, humanYAP-Signaling ProteinsACTR2COPDNuclear membrane ruptureSarcopeniaSenescenceYAP/TAZ

Identifiers

PMID40075503
PMCPMC11905641

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.